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1 ted a significant suppression in spontaneous mammary tumorigenesis.
2 K activation and P50 phosphorylation causing mammary tumorigenesis.
3 essor of oncogenic TGF-beta signaling during mammary tumorigenesis.
4 the oncogenic activities of TGF-beta during mammary tumorigenesis.
5 geted anticancer therapy in a mouse model of mammary tumorigenesis.
6 n of downstream effectors and ErbB2-mediated mammary tumorigenesis.
7 egulated during the process of CR-1-mediated mammary tumorigenesis.
8 ptibility gene 1 (BRCA1) plays a key role in mammary tumorigenesis.
9 at tissue overexpression of IGF-1 stimulates mammary tumorigenesis.
10 2/neu transgenes, Hoxb7 plays a dual role in mammary tumorigenesis.
11 ssively restricted to the vasculature during mammary tumorigenesis.
12 of mammary alveolar/lobular development and mammary tumorigenesis.
13 (OGG1) in the PyMT transgenic mouse model of mammary tumorigenesis.
14 eventing the superantigen (Sag) response and mammary tumorigenesis.
15 nergized with defective apoptosis to promote mammary tumorigenesis.
16 study stromal TGF-beta and HGF signaling in mammary tumorigenesis.
17 ates a requirement for Akt1 in ErbB2-induced mammary tumorigenesis.
18 at cyclin D1 was required for ErbB-2-induced mammary tumorigenesis.
19 markedly with oncogenic ras or neu in murine mammary tumorigenesis.
20 erates with the neu-ras oncogenic pathway in mammary tumorigenesis.
21 cancer tissue and in a mouse model of ErbB2 mammary tumorigenesis.
22 cur early in the process of estrogen-induced mammary tumorigenesis.
23 e antagonist mifepristone (RU 486) prevented mammary tumorigenesis.
24 d in the protection against estrogen-induced mammary tumorigenesis.
25 for the active role of MMPs in Wnt1-induced mammary tumorigenesis.
26 ts exhibit parity-induced protection against mammary tumorigenesis.
27 on and contributes to the hormonal impact on mammary tumorigenesis.
28 ffect against mammary hyperplasia as well as mammary tumorigenesis.
29 ed, indicating that MET and MYC cooperate in mammary tumorigenesis.
30 nd indispensable role in MMTV-PyV MT-induced mammary tumorigenesis.
31 ed nonreceptor tyrosine kinase implicated in mammary tumorigenesis.
32 e that Cox-2 contributes to HER2/neu-induced mammary tumorigenesis.
33 e during early events of ErbB2/Neu-initiated mammary tumorigenesis.
34 ways may be a significant determinant during mammary tumorigenesis.
35 aling and thus stimulates hormone-responsive mammary tumorigenesis.
36 epair machinery as important contributors to mammary tumorigenesis.
37 umor suppressor role of E2F2 in Myc-mediated mammary tumorigenesis.
38 reast cancers, is capable of contributing to mammary tumorigenesis.
39 ntiation, an effect that could contribute to mammary tumorigenesis.
40 sity at the Ink4a/Arf locus in ErbB2-induced mammary tumorigenesis.
41 t that progesterone has an important role in mammary tumorigenesis.
42 y early mutational target in c-erbB2-induced mammary tumorigenesis.
43 for Brca1 or Brca2 is highly susceptible to mammary tumorigenesis.
44 ent DCIS and, thus, may be an early event in mammary tumorigenesis.
45 ling through PGE2 receptors is important for mammary tumorigenesis.
46 f both Apc and Tcf-1 have been implicated in mammary tumorigenesis.
47 curring in most traditional models of murine mammary tumorigenesis.
48 us insertion results in pregnancy-responsive mammary tumorigenesis.
49 are important in modulating Neu function in mammary tumorigenesis.
50 mber of oncogenes, that ultimately result in mammary tumorigenesis.
51 in cell adhesion may be very early events in mammary tumorigenesis.
52 BRCA2 is a tumor suppressor gene involved in mammary tumorigenesis.
53 iated with and is capable of contributing to mammary tumorigenesis.
54 ammation in the mammary fat pad and promoted mammary tumorigenesis.
55 rstanding of the molecular mechanisms of rat mammary tumorigenesis.
56 eractions of biochemical pathways leading to mammary tumorigenesis.
57 studies that progesterone markedly enhances mammary tumorigenesis.
58 impact the progression of TGFalpha-mandated mammary tumorigenesis.
59 Sv, suggests a genetic predisposition toward mammary tumorigenesis.
60 sis for the role of p53 in the regulation of mammary tumorigenesis.
61 (Fgf8) as a possible proto-oncogene in mouse mammary tumorigenesis.
62 contributing to the fat-induced promotion of mammary tumorigenesis.
63 ted in a 50% reduction of chemically induced mammary tumorigenesis.
64 o determine the effect of MAT on neu-induced mammary tumorigenesis.
65 ine the specific effects of this mutation on mammary tumorigenesis.
66 ammary epithelium contributes to early-stage mammary tumorigenesis.
67 eful in the investigation of early events in mammary tumorigenesis.
68 C3(1) 5'-flanking region display multistage mammary tumorigenesis.
69 nstitutively free to function in its role in mammary tumorigenesis.
70 ng the CDK-cyclin D1-PELP1 axis in promoting mammary tumorigenesis.
71 ive oxygen species (ROS) on the induction of mammary tumorigenesis.
72 lpha) activity is required for ErbB2-induced mammary tumorigenesis.
73 (Neu DeLetion mutant) model of ErbB2-induced mammary tumorigenesis.
74 he pathophysiologic significance of FABP5 in mammary tumorigenesis.
75 ortunity to study the importance of c-Src in mammary tumorigenesis.
76 of mammary alveolar/lobular development and mammary tumorigenesis.
77 opment and that it has a suppressive role in mammary tumorigenesis.
78 d in the protection against estrogen-induced mammary tumorigenesis.
79 errant mammary gland development and induces mammary tumorigenesis.
80 t DDE exposure would promote, but not cause, mammary tumorigenesis.
81 f mammary epithelial cells and also promotes mammary tumorigenesis.
82 eficient mouse model substantially curtailed mammary tumorigenesis.
83 r probing the cellular signaling pathways in mammary tumorigenesis.
84 r activation and is an important mediator of mammary tumorigenesis.
85 s a key role in both hereditary and sporadic mammary tumorigenesis.
86 with the Wnt/beta-catenin pathway to promote mammary tumorigenesis.
87 ice, iFGFR1 activation dramatically enhanced mammary tumorigenesis.
88 1 phosphatase in the DNA damage response and mammary tumorigenesis.
89 ine a direct contribution of this pathway in mammary tumorigenesis.
90 timulated by SnoN was insufficient to induce mammary tumorigenesis.
91 cesses may contribute to NF-kappaB-dependent mammary tumorigenesis.
92 MEC NF-kappaB contributes to mammary tumorigenesis.
93 a model system to study the role for Pak4 in mammary tumorigenesis.
94 lation of Jak2 protects against the onset of mammary tumorigenesis.
95 of the main estrogen metabolites that induce mammary tumorigenesis and (ii) ROS-mediated signaling le
96 ved in IFN-gamma gene down-regulation during mammary tumorigenesis and contributes to the generalized
98 ssion of d16HER2 is sufficient to accelerate mammary tumorigenesis and improve the response to trastu
99 C3H mouse mammary tumor virus (MMTV)-induced mammary tumorigenesis and lack major histocompatibility
100 Here, we examined the role of caveolin-1 in mammary tumorigenesis and lung metastasis using a molecu
102 s responsible in part for the suppression of mammary tumorigenesis and metastasis caused by inhibitio
103 ta.neu transgenic mice exhibited accelerated mammary tumorigenesis and metastasis compared with MMTV-
104 tor beta (TGF-beta) signaling on Neu-induced mammary tumorigenesis and metastasis was examined with t
112 xpression of 14-3-3zeta has a causal role in mammary tumorigenesis and progression, acting through mi
113 ongly synergizes with both c-MYC and Wnt1 in mammary tumorigenesis and promotes the progression of tu
114 Loss of miR-10b delays oncogene-induced mammary tumorigenesis and suppresses epithelial-mesenchy
115 genetic silencing of EcSOD may contribute to mammary tumorigenesis and that restoring the extracellul
117 of E2F1 and E2F3 in ErbB2- or Myc-triggered mammary tumorigenesis, and a tumor suppressor role of E2
119 ect role of PPARdelta in the pathogenesis of mammary tumorigenesis, and suggest a rationale for thera
120 we found that ERalpha and ERbeta expression, mammary tumorigenesis, and survival are energy balance d
121 f one copy of APC promotes oncogene-mediated mammary tumorigenesis, Apc(Min/+) mice were crossed with
122 equirement for Cdk2 in LMW-cyclin E-mediated mammary tumorigenesis, arguing that human breast tumors
123 an breast cancers and has been implicated in mammary tumorigenesis as well as in mediating aggressive
124 oinsufficient tumor suppressor mechanism for mammary tumorigenesis, as the essential autophagy regula
125 zed SCRIB functions as a neomorph to promote mammary tumorigenesis by affecting subcellular localizat
126 cooperativity between neu and mutant p53 in mammary tumorigenesis by creating bitransgenic mice carr
128 onstrated that MTDH plays a critical role in mammary tumorigenesis by regulating oncogene-induced exp
130 Although loss of Lkb1 alone does not promote mammary tumorigenesis, combination of Lkb1 deficiency wi
131 nic models, whereas loss of E2f2 accelerated mammary tumorigenesis driven by Myc-overexpression.
132 Mtv-null mice restrict MMTV replication and mammary tumorigenesis even after a robust Sag response.
133 protection against methylnitrosourea-induced mammary tumorigenesis following treatment with pregnancy
134 In this study, we generated a mouse model of mammary tumorigenesis harboring the MMTV-HER2 oncogene a
136 f p62 in the pathophysiology of HER2-induced mammary tumorigenesis has not yet been investigated.
137 esterone receptor (PR) and progestins affect mammary tumorigenesis; however, the relative contributio
138 mice to ascertain the role of Id1 and Id3 in mammary tumorigenesis in a more physiologically relevant
139 mammary epithelium significantly suppresses mammary tumorigenesis in a well-characterized breast can
140 , and treating with anti-progesterone delays mammary tumorigenesis in Brca1/p53 conditional knock-out
142 g individual E2fs in mice on ErbB2-triggered mammary tumorigenesis in comparison to a comparable Myc-
143 deletion of Vhl was not sufficient to induce mammary tumorigenesis in dams bred continuously for up t
144 PTEN can partially inhibit the Wnt-1-induced mammary tumorigenesis in early neoplastic stages by bloc
145 k protein 70 (Hsp72) have been implicated in mammary tumorigenesis in histological investigations of
146 re dynamics and telomerase activation during mammary tumorigenesis in mice carrying a mouse mammary t
148 We have previously shown that c-MYC-induced mammary tumorigenesis in mice proceeds via a preferred s
149 ncer risk, and inactivation of chk2 enhances mammary tumorigenesis in mice with targeted inactivation
150 AP-p53(172H)) could accelerate ErbB2-induced mammary tumorigenesis in mice, but was not tumorigenic o
154 mechanisms regulated by TFAP2C, we examined mammary tumorigenesis in MMTV-Neu transgenic female mice
156 Diet-stimulated ductal growth also increased mammary tumorigenesis in ovariectomized polyomavirus mid
158 d the ability of tamoxifen to block or delay mammary tumorigenesis in several versions of this model.
159 am), inhibit estrogen-induced DNA damage and mammary tumorigenesis in the aromatase transgenic (Arom)
162 target of rapamycin inhibitor, rapamycin, on mammary tumorigenesis in transgenic mice bearing an acti
165 genetic ablation of p62 delays HER2-induced mammary tumorigenesis in tumor cell allografts in nude m
166 nd cellular mechanisms by which FAK promotes mammary tumorigenesis in vivo are not well understood.
167 l NF-kappaB activity enhances ErbB2-mediated mammary tumorigenesis in vivo by promoting both growth a
179 ly we have used MMTV infection to accelerate mammary tumorigenesis in Wnt1 transgenic mice in order t
180 suggest that activation of PDK1 can lead to mammary tumorigenesis, in part through PKCalpha, and tha
181 rus middle T oncogene-induced (PyMT-induced) mammary tumorigenesis, increased survival, and reduction
182 nfer a lasting protection against subsequent mammary tumorigenesis induced by methylnitrosourea.
183 mice show substantially prolonged latency in mammary tumorigenesis induced by MMTV-H-ras or MMTV-neu
184 t Hunk is required for c-myc suppression and mammary tumorigenesis induced by phosphatase and tensin
185 t cooperation of the FGF and Wnt pathways in mammary tumorigenesis is based on the activation of prot
188 e show that increased Cdc7 expression during mammary tumorigenesis is linked to Her2-overexpressing a
189 ve and cooperative role for c-Myc and Ras in mammary tumorigenesis is well documented, their ability
190 show that hormone-induced protection against mammary tumorigenesis is widely conserved among divergen
191 nce that KLF4 has a potent oncogenic role in mammary tumorigenesis likely by maintaining stem cell-li
193 role of matrix metalloproteinase 7 (MMP7) in mammary tumorigenesis, MMP7 was expressed in the normal
195 s cancer chemopreventive effects in skin and mammary tumorigenesis models and that additional studies
196 terozygous for p53 synergistically increases mammary tumorigenesis more than that in mice carrying ei
197 ow women's therapies influence all stages of mammary tumorigenesis, particularly for assessing their
198 hese findings demonstrate that c-MYC-induced mammary tumorigenesis proceeds through a preferred secon
199 ntrast, we now demonstrate that Wnt1-induced mammary tumorigenesis proceeds via a pathway that prefer
200 lity of cyclin E to play a causative role in mammary tumorigenesis, regulatory sequences from the ovi
207 sm underlying the protein's possible role in mammary tumorigenesis, Sca-1 expression was examined in
209 the promotional role of ovarian hormones on mammary tumorigenesis, suggesting that AIB1 and ovarian
210 tively, our data reveal that IQGAP1 enhances mammary tumorigenesis, suggesting that it may be a targe
211 k2 protects against the onset of PRL-induced mammary tumorigenesis, suggesting that targeting this ki
212 NE knockout in the C3(1)TAg mouse model of mammary tumorigenesis suppressed proliferation and reduc
214 cell renewal, luminal cell differentiation, mammary tumorigenesis, tamoxifen sensitivity and chemoth
215 te that, in the setting of viral oncoprotein mammary tumorigenesis, telomerase-dependent telomere mai
217 sts produce diverse, yet profound effects on mammary tumorigenesis that give rise to distinctive hist
219 vidence that p62 contributes to HER2-induced mammary tumorigenesis through multiple signaling pathway
220 R2/Neu and ACTR may synergize to orchestrate mammary tumorigenesis through the dysregulation of the t
221 The precise sequence of events that enable mammary tumorigenesis to convert transforming growth fac
222 ugh AIB1 deficiency significantly suppressed mammary tumorigenesis under all of the concentrations of
223 done to define the role of fetuin-A (Fet) in mammary tumorigenesis using the polyoma middle T antigen
224 ects of MAT expression on the development of mammary tumorigenesis using transgenic mice that express
225 Oncogenes Neu/HER2/ErbB2 and Ras can induce mammary tumorigenesis via upregulation of cyclin D1.
229 importance of cyclin D1 in ERalpha-mediated mammary tumorigenesis, we crossed ERalpha-overexpressing
230 ed to be a key mediator for ErbB2-associated mammary tumorigenesis, we deleted Jak2 from ErbB2-expres
233 r signal-regulated kinases (ERK) 1/2 promote mammary tumorigenesis, we examined the real-time behavio
234 equirement for Cdk2 in LMW-cyclin E-mediated mammary tumorigenesis, we generated transgenic mice, whi
235 To examine whether AIB3 reduction affects mammary tumorigenesis, we generated wild-type mouse mamm
236 le of CSF-1 or its receptor in initiation of mammary tumorigenesis, we have generated two independent
237 ne whether CK2 overexpression contributes to mammary tumorigenesis, we have performed comparative stu
238 hat may be causally involved in MMTV-induced mammary tumorigenesis, we identified 60 sites of provira
239 TNFRSF11A (also known as RANK) contribute to mammary tumorigenesis, we investigated a role for this p
241 transgenic mouse models for HER2/neu-induced mammary tumorigenesis, we report that Hunk is required f
242 entify genes that cooperate with TGFalpha in mammary tumorigenesis, we used a retroviral insertion ap
243 insic susceptibilities to carcinogen-induced mammary tumorigenesis were each shown to display signifi
244 n this study, the effects of black cohosh on mammary tumorigenesis were investigated in the MMTV-neu
245 ) and reduced N-methyl-N-nitrosourea-induced mammary tumorigenesis when administered to female Spragu
246 man breast cancer and is capable of inducing mammary tumorigenesis when overexpressed in transgenic m
247 knockout of FIP200 significantly suppressed mammary tumorigenesis, which was accompanied by accumula
248 f activated Her2/Neu resulted in accelerated mammary tumorigenesis with enhanced metastatic potential
249 tumor incidence and triggered early onset of mammary tumorigenesis with increased lung metastasis in
250 ygous status significantly accelerated mouse mammary tumorigenesis with reduced apoptosis and increas
251 three-dimensional matrices, a mouse model of mammary tumorigenesis with vinculin mutants, and a novel
252 els and an autochthonous transgenic model of mammary tumorigenesis, with less overall tumour cell dea
253 to a tumor promoter occurs frequently during mammary tumorigenesis, yet the molecular mechanisms unde
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